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Interleukin-1beta mediates the extra-intestinal thrombosis associated with experimental colitis
Hideo Yoshida1, Janice Russell, Elena Y Senchenkova
1Eiju General Hospital, Tokyo, Japan.
The American Journal of Pathology
|October 26, 2010
Summary
Interleukin-1 beta (IL-1β) drives extra-intestinal blood clots in inflammatory bowel diseases (IBD). Blocking IL-1β or its receptor reduces thrombosis risk in colitis models.
Area of Science:
- Vascular Biology
- Immunology
- Gastroenterology
Background:
- Inflammatory bowel diseases (IBD) increase the risk of blood clots (thromboembolism) in areas outside the intestines.
- Cytokines involved in IBD pathogenesis may influence coagulation, but their role in extra-intestinal thrombosis is not fully understood.
Purpose of the Study:
- To investigate the role of interleukin-1 beta (IL-1β) in promoting extra-intestinal thrombosis in a mouse model of dextran sodium sulfate (DSS)-induced colitis.
Main Methods:
- Measured IL-1β levels in plasma, colon, and skeletal muscle of wild-type (WT) and colitic mice.
- Induced microvascular thrombosis in cremaster muscle using a light/dye injury model.
- Assessed the impact of exogenous IL-1β on thrombus formation in WT mice.
- Evaluated DSS-induced thrombogenesis in WT mice treated with an IL-1β antibody and in IL-1 receptor-deficient (IL-1r(-/-)) mice.
Main Results:
- DSS-induced colitis in WT mice led to increased thrombus formation in arterioles.
- Elevated IL-1β concentrations were observed in inflamed colon and skeletal muscle tissues.
- Exogenous IL-1β administration enhanced thrombosis in a dose-dependent manner.
- Treatment with an IL-1β antibody or using IL-1r(-/-) mice significantly reduced thrombotic responses in DSS-induced colitis.
Conclusions:
- Interleukin-1 beta (IL-1β) is implicated as a key mediator of enhanced microvascular thrombosis in extra-intestinal tissues during colonic inflammation.
- Targeting IL-1β may offer a therapeutic strategy to mitigate the thrombotic complications associated with inflammatory bowel diseases.
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